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微孢子虫感染对亚洲蜜蜂蔗糖溶液消耗、抗氧化酶活性、细胞结构和寿命的广泛影响。

Extensive influence of microsporidian infection on sucrose solution consumption, antioxidant enzyme activity, cell structure, and lifespan of Asian honeybees.

作者信息

Fan Xiaoxue, Zhao Haodong, Zang He, Dong Shunan, Qiu Jianfeng, Song Yuxuan, Li Kunze, Jiang Haibin, Wu Ying, Lü Yang, Zhou Dingding, Fu Zhongmin, Chen Dafu, Guo Rui

机构信息

College of Bee Science and Biomedicine, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.

National & Local United Engineering Laboratory of Natural Biotoxin, Fujian Agriculture and Forestry University, Fuzhou, Fujian, China.

出版信息

Front Immunol. 2024 Nov 19;15:1404766. doi: 10.3389/fimmu.2024.1404766. eCollection 2024.

DOI:10.3389/fimmu.2024.1404766
PMID:39628478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11611804/
Abstract

is the original host of ceranae, a widespread fungal parasite that causes bee nosemosis, which severely threatens the health of bee colonies and the sustainable development of the apiculture industry. To evaluate the impact of infection on workers, spores were purified and used to inoculate newly emerged workers to evaluate the effects of infection. This was followed by an in-depth investigation of spore load and host sucrose solution consumption. Activities of four major antioxidant enzymes (SOD, PPO, CAT, and GST) were determined. Paraffin sections of the host midgut tissue were prepared and subjected to microscopic observation. The survival rates of -inoculated and uninoculated workers were analyzed. The results showed that spore load gradually increased and peaked at 12 dpi. The consumption of workers in the -inoculated group was extremely significant higher ( < 0.0001) than that of workers in the un-inoculated group. The results of antioxidant enzyme activity were suggestive of positive host defense via catalase (CAT) and glutathione-S-transferase (GST) in the middle stage of infection, as well as the negative fungal impact on superoxide dismutase (SOD) and polyphenol oxidase (PPO) at the whole stage of infection, reflecting the complex host-parasite interaction. Additionally, we observed a disruption in the structure of the host midgut epithelial cells. Moreover, the survival rate of workers in -inoculated groups was nearly always lower than that of workers in the uninoculated groups. These results demonstrate a consistent increase in spore load with the proliferation of , leading to persistent energetic stress and midgut epithelial cell structural damage to the host, ultimately resulting in a shortened lifespan for the host. Our findings enhance the current understanding of the interactions between and as well as provide a solid basis for exploring the mechanisms underlying host response and infection.

摘要

是蜜蜂微孢子虫的原始宿主,蜜蜂微孢子虫是一种广泛传播的真菌寄生虫,可导致蜜蜂微孢子虫病,严重威胁蜂群健康和养蜂业的可持续发展。为了评估感染对工蜂的影响,对孢子进行了纯化,并用于接种新羽化的工蜂以评估感染的影响。随后深入研究了孢子载量和宿主蔗糖溶液消耗量。测定了四种主要抗氧化酶(超氧化物歧化酶、多酚氧化酶、过氧化氢酶和谷胱甘肽 - S - 转移酶)的活性。制备了宿主中肠组织的石蜡切片并进行显微镜观察。分析了接种和未接种工蜂的存活率。结果表明,孢子载量逐渐增加,并在接种后12天达到峰值。接种组工蜂的消耗量极显著高于未接种组(<0.0001)。抗氧化酶活性结果表明,在感染中期宿主通过过氧化氢酶(CAT)和谷胱甘肽 - S - 转移酶(GST)进行积极防御,以及在感染全过程真菌对超氧化物歧化酶(SOD)和多酚氧化酶(PPO)产生负面影响,反映了宿主 - 寄生虫之间复杂的相互作用。此外,我们观察到宿主中肠上皮细胞结构遭到破坏。而且,接种组工蜂的存活率几乎总是低于未接种组。这些结果表明,随着蜜蜂微孢子虫的增殖,孢子载量持续增加,导致宿主持续的能量应激和中肠上皮细胞结构损伤,最终导致宿主寿命缩短。我们的研究结果加深了目前对蜜蜂微孢子虫与宿主之间相互作用的理解,并为探索宿主反应和蜜蜂微孢子虫感染的潜在机制提供了坚实基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/0843f7655be5/fimmu-15-1404766-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/8391f9b13f45/fimmu-15-1404766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/9914f37e0a96/fimmu-15-1404766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/305eae4b9efb/fimmu-15-1404766-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/61925d7ce09d/fimmu-15-1404766-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/577af5893aa6/fimmu-15-1404766-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/e0505f1f851f/fimmu-15-1404766-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/48b3d3b09a49/fimmu-15-1404766-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/0843f7655be5/fimmu-15-1404766-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/8391f9b13f45/fimmu-15-1404766-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/9914f37e0a96/fimmu-15-1404766-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/305eae4b9efb/fimmu-15-1404766-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/61925d7ce09d/fimmu-15-1404766-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/577af5893aa6/fimmu-15-1404766-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/e0505f1f851f/fimmu-15-1404766-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/48b3d3b09a49/fimmu-15-1404766-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a66/11611804/0843f7655be5/fimmu-15-1404766-g008.jpg

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